The present invention relates generally to implantable cardioverter-defibrillators, and more particularly, to a method of using electrical energy to produce temporary conduction block in a local region of the patient""s myocardium which will disrupt a reentry pathway through which an a trial or ventricular tachycardia (or other type of arrhythmia) is initiated and perpetuated, thereby resulting in cardioversion or defibrillation.
Ventricular fibrillation (VF) has been defined as a xe2x80x9cchaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge.xe2x80x9d The resulting uncoordinated excitation and contraction of the ventricles is incapable of pumping blood. Therefore, blood pressure drops rapidly and approaches the mean circulatory pressure within approximately 4-10 seconds. Death generally occurs if the VF is not terminated within 5-10 minutes.
Under normal circumstances, the excitation wave which causes ventricular contraction passes across the ventricle before the myocardial cells become reexcitable (i.e., while the myocardial cells are still refractory and insusceptible to activation). Therefore, the excitation wave dies out and the ventricle remains quiescent until the next impulse arrives through the conduction system. However, if a conduction slowing or block occurs so that cells that have previously been stimulated recover excitability before the excitation wave reaches the area, then repetitive reentrant excitation can occur, leading to VF.
Implantable cardioverter-defibrillators (ICDs) have revolutionized therapy for patients with sustained ventricular tachycardias. ICDs monitor the intrinsic electrical activity of the patient""s heart in accordance with a detection or diagnostic algorithm by analyzing electrogram (EGMs) generated by sensing electrodes positioned in the right ventricular apex of the patient""s heart. Current-generation ICDs are capable of delivering various types or levels of cardiac therapy, depending upon the type of abnormal cardiac electrical activity which is detected (i.e., depending upon the diagnosis). This capability is commonly referred to in the art as xe2x80x9ctiered therapyxe2x80x9d, the basic idea of which is to xe2x80x9cmake the punishment fit the crimexe2x80x9d.
The first type or level of therapy is antitachycardia (also, bradycardia) pacing (ATP), in which a low level of electrical energy (generally between millionths to thousandths of a joule) is delivered to the patient""s heart (via a transvenous, non-thoracotomy lead/electrode system) in order to correct detected episodes of tachycardia (or bradycardia). The second type or level of therapy is cardioversion, in which an intermediate level of electrical energy (generally between 1-5 joules) is delivered to the patient""s heart (via the lead/electrode system) to terminate a detected episode of ventricular tachyarrhythmia (e.g., a detected heart beat in the range of 130-190 beats/minute) or an ongoing episode of tachycardia that ATP therapy failed to terminate. The third type or level of therapy is defibrillation, in which a high level of electrical energy (generally above 15 joules) is delivered to the patient""s heart (via the lead/electrode system) in order to terminate a detected sudden episode of ventricular fibrillation or an episode of ventricular tachycardia which has degraded into ventricular fibrillation due to failure of cardioversion or ATP therapy. The primary goal is to prevent or terminate ventricular tachyarrhythmias in the most efficacious manner while simultaneously minimizing the amount of electrical energy required to do so. This enables the size of the ICD to be minimized and the mean time between replacements of the ICD to be extended, which decreases patient discomfort both at the time of implant and during wear.
Although ICDs have been largely effective for ventricular defibrillation, electrical therapy of complex arrhythmias such as a trial fibrillation is presently difficult. While high energy defibrillation shocks such as those used for ventricular defibrillation are often effective, they produce intolerable pain levels, requiring sedation, if delivered to terminate non-life threatening a trial arrhythmias. Thus, they are impractical for such a trial arrhythmias in an automatic implantable device. Low energy therapies have not yet been realized due to the limited regions of capture associated with point stimulation.
An alternative is ablative therapy. There are two types of ablative therapy, namely, surgical and catheter ablative therapy. The aim of either type of ablative therapy is to permanently destroy (irreversibly damage) the myocardium which constitutes the critical part of the reentrant circuit of the ventricular or a trial tachycardia which is required to sustain or perpetuate the ventricular or a trial tachycardia. In other words, the ablation of the critical region of the myocardium acts to permanently eliminate the conduction or impulse formation through the reentrant pathway which is required to sustain or perpetuate the ventricular or a trial tachycardia. Successful ablation is critically dependent on the ability to localize the involved myocardium necessary to initiate and perpetuate the ventricular or a trial tachycardia. Diagnostic techniques used to localize the reentry circuit include analysis of a 12-lead ECG, catheter mapping during a trial or ventricular tachycardia, and pace mapping. Once the site of origin of ventricular or a trial tachycardia is localized, ablative procedures (surgical or catheter directed) can be performed.
In the catheter ablation approach, catheter-based electrodes are used to permanently disable myocardium tissue adjacent to the electrode without affecting more distant tissue. See, xe2x80x9cBasic Aspects of Radiofrequency Catheter Ablationxe2x80x9d, S. Nath et al., J. Cardiovascular Electrophysiology, Oct. 1994, p. 863, the disclosure of which is incorporated herein by reference, and xe2x80x9cRadiofrequency Catheter Ablation of Cardiac Arrhythmias: Basic Concepts and Clinical Applicationsxe2x80x9d, DiMarco and Prystowsky, eds., AHA Monograph Series, Futura Publishing Company, NY, 1995, the disclosure of which is also incorporated herein by reference.
Using RF energy (500-1000 kHz, 15-50 W, 100-800 J, 30-75 V rms and 0.1-1 A rms, for 10-60 sec.), tissue extending several mm from the electrode is heated to 65-100xc2x0 C. This produces permanent lesions that block reentry or disable the AV node. Particularly in the case of atrial fibrillation, specific anatomical structures are often associated with reentry pathways required to sustain arrhythmias. Work is ongoing to develop limited ablation procedures that will permanently block these critical conduction pathways. As a result, the incidence of arrhythmias may decrease and/or the arrhythmias may be better organized, thereby leading to a higher degree of success with low energy shock therapies. One example of a critical isthmus of conduction for atrial flutter cited by Lesh and co-workers, is found in the lower right atrium extending from the inferior vena cava to the coronary sinus ostium bordered by the eustachian ridge (ER) and the tricuspid annulus (TA). See, xe2x80x9cConduction barriers in Human Atrial Flutterxe2x80x9d, Olgin et al., JCE, Vol. 7, Nov. 1996, p. 1112, the disclosure of which is also incorporated herein by reference. Lesh et al. also speculate that any lesion connecting the ER/crista terminals and the TA could interrupt the atrial flutter reentrant circuit. Although the reentrant pathways for AF are more complex and possibly shorter and more numerous, some success has been achieved with the use of multiple lesions to cure AF.
In spite of the advancements in ablative therapy discussed above, there are significant drawbacks and shortcomings of ablative therapy. Namely, in addition to the fact that ablative therapy carries with it a significant mortality and morbidity risk, it produces permanent myocardial damage.
Based on the above and foregoing, it can be appreciated that there presently exists a need in the art for a method for terminating atrial (and ventricular) tachyarrhythmias which overcomes the above-discussed drawbacks and shortcomings of the presently available technology. More particularly, there is a need in the art for a method for terminating atrial (and ventricular) tachyarrhythmias which uses relatively low energy electrical stimuli and does not cause permanent myocardial damage. The present invention fulfills this need in the art.
The present invention encompasses a method for treating arrhythmias which includes the steps of detecting an arrhythmia, and, in response to detection of the arrhythmia, delivering electrical energy to a targeted part of myocardial tissue in such a manner as to create a transient conduction block in the targeted part of the myocardial tissue without causing permanent damage to the targeted part of the myocardial tissue. The electrical energy can be continuous (e.g., sinusoidal) or pulsed RF, or continuous or pulsed DC. The detected arrhythmia can be atrial fibrillation, atrial flutter, ventricular fibrillation, or other type of arrhythmia. The targeted part of the myocardial tissue constitutes a critical part of the reentrant pathway or reentrant circuit required to sustain the detected arrhythmia. The electrical energy is preferably delivered via a catheter-based electrode which is in direct contact with the targeted part of the myocardial tissue, for either a prescribed period of time or until the arrhythmia is no longer detected (i.e., is terminated). In the former case, the prescribed period of time can be either sufficient to ensure that the arrhythmia can no longer be sustained, or sufficient to ensure that the arrhythmia is organized well enough to be terminated with additional low energy cardioversion/defibrillation therapy (such as a biphasic shock or pulse train).
Further, in a first alternative embodiment of the method of the present invention, a shock (or other form of cardioversion or defibrillation therapy) can be delivered first, and then, if necessary (e.g., if it is detected that the fibrillation has not been terminated), electrical energy can be delivered to a targeted part of the myocardial tissue in order to create a transient conduction block in the targeted part of the myocardial tissue.
In a second alternative embodiment of the method of the present invention, electrical energy is delivered to a targeted part of the myocardial tissue in order to create a first transient conduction block in the targeted part of the myocardial tissue, then a shock (or other form of cardioversion or defibrillation therapy) can be delivered, and then, if necessary (e.g., if it is detected that the fibrillation has not been terminated), electrical energy can again be delivered to the targeted part of the myocardial tissue in order to create a second transient conduction block in the targeted part of the myocardial tissue.
The method of the present invention (any embodiment) is preferably carried out by using an automatic implantable defibrillator.